Koh Yoshida

Functional roles of the superior laryngeal nerve afferents in electrically induced vocalization in anesthetized cats

Our purpose was to elucidate the functional roles of the laryngeal afferents in controlling vocalization. We investigated the effects of laryngeal deafferentation (sectioning the internal branch of the superior laryngeal nerve (ISLN)) on respiration and voice quality during electrically-induced vocalization in twelve ketamine anesthetized cats. Co-ordinated vocal activity was obtained by electrical stimulation to the pontine call site. After the bilateral ISLN section, the respiratory, expiratory and inspiratory durations during induced vocalization became 0.56 +/- 0.15, 0.44 +/- 0.12 and 0.67 +/- 0.19 (mean +/- S.D., n = 9) times, respectively, compared with those before the ISLN section. A decrease in respiratory duration was also observed when local anesthetics were applied to the laryngeal mucosa. The laryngeal deafferentation increased the degree of hoarseness with a decrease in the fundamental frequency. Since the laryngeal deafferentation caused a decrease in the intralaryngeal adductor activities, it was suspected that the voice quality change was partly caused by the reduction in adductor activities. It was thus concluded that feedback via laryngeal afferents plays an important role in controlling vocalization.

Influences of laryngeal afferent inputs on intralaryngeal muscle activity during vocalization in the cat

The present study was undertaken to elucidate the possible role of the laryngeal afferent inputs in the regulation of intralaryngeal muscle activity during vocalization. We studied the influences of airflow and/or pressure applied to the larynx on intralaryngeal muscle activity during vocalization in ketamine-anesthetized cats. Vocalization was induced by airflow applied to the upper airway, which was isolated from the lower airway, during pontine call site stimulation. When the upper airway was open to the atmosphere through the nostrils and mouth, the airflow increased not only the vocal fold adductor and tensor activities but also the duration of these activities. The adductor and tensor activities were increased suddenly at a critical subglottic pressure level equivalent to the subglottic pressure threshold for vocalization. These effects were significantly reduced by sectioning of the internal branch of the superior laryngeal nerve or by lidocaine application to the laryngeal mucosa. Sustained pressure applied to the isolated upper airway, when the mouth and nostrils were occluded, did not affect adductor or tensor activities. These results indicate that the afferent inputs evoked by vocal fold stretching or vibration play an important role in the motor control of intralaryngeal and respiratory muscles during vocalization.

Role of pulmonary afferent inputs in vocal on-switch in the cat

The purpose of this paper is to elucidate the possible role of pulmonary afferent inputs in triggering inspiratory-vocal (I-V) and Vocal-inspiratory (V-I) transitions during periaqueductal gray (PAG)-induced vocalization. Under ketamine anesthesia, we investigated the effects of changes in pulmonary afferent inputs on the PAG-induced vocal motor pattern by transection and electrical stimulation of the cervical vagus nerve in non-paralyzed cats and by lung inflation and deflation in paralyzed cats. After bilateral vagotomy, PAG stimulation induced apneusis; strong suppression of the I-V transition disrupted the vocal rhythmicity. Electrical stimulation of the central end of the cut vagus nerve during PAG stimulation immediately caused an I-V transition. In paralyzed cats during the withholding of lung inflation, the I-V transition was also suppressed during PAG stimulation. Lung inflation during PAG stimulation caused a phase switch from inspiration to fictive vocalization, i.e. I-V transition. In contrast, this fictive vocal phase maintained by lung inflation was terminated by lung deflation, i.e. V-I transition. These findings suggest that pulmonary vagal afferent feedback plays an important role in triggering and terminating vocalization.

Frequency and clinical features of patients with sensorineural hearing loss associated with the A3243G mutation of the mitochondrial DNA in otorhinolaryngic clinics

AbstractThe A3243G mutation of the mitochondrial gene is a cause of maternally inherited diabetes and deafness. The aim of this study was to evaluate the frequency and clinical features of this mutation in patients with sensorineural hearing loss (SNHL) in otorhinolaryngic clinics. The frequency of the A3243G mutation in 230 patients with SNHL was 1.74% (4/230). Three of the four patients had diabetes mellitus (DM) and were already aware that they had the mutation. The other had cardiomyopathy but not DM, and proved to have the mutation in this study. The frequency of the mutation was 12.9% (4/31) in patients with a family history of possible maternal inheritance of SNHL, 10.3% (3/29) in patients with DM, and 50% (3/6) in patients with both. The age of onset of SNHL in these patients and their families was between their teens and their forties. The chance of diagnosing the A3243G mutation in patients with SNHL in otorhinolaryngic clinics is probably less than 1%. Association of DM, cardiomyopathy, a family history of possible maternal inheritance of SNHL, and an onset of SNHL between the teens and the forties are signs suggesting the mutation. These signs provide us with a reason for genetic testing for the mutation.

Increased nasal mucosal blood flow, airway resistance and secretion induced by electrical stimulation of the superior salivatory nucleus in cats.

We studied the effects of electrical stimulation of the superior salivatory nucleus (SSN) on the nasal blood flow, nasal airway resistance, and nasal secretion in ketamine or pentobarbital anesthetized cats. The blood flow of the nasal mucosa was measured by laser Doppler flowmetry. Similar to the effects of stimulation of the parasympathetic nerve innervating the nasal mucosa, the SSN stimulation increased the nasal blood flow, nasal airway resistance, and nasal secretion on the ipsilateral side. These responses were not accompanied by changes in contralateral nasal blood flow, ipsilateral forelimb blood flow, blood pressure, or orofacial movement. Atropine administration partially inhibited the SSN-induced nasal vasodilation without interfering with the effect on the nasal airway resistance. This vasodilatation was not affected by sympathectomy or guanethidine administration, but it was abolished by hexamethonium administration. It is suspected that the cells in the SSN control both nasal vasodilatation and secretion, and that the SSN output fibers responsible for the nasal parasympathetic control consist of both cholinergic and non-cholinergic fibers.

Does nitric oxide mediate plasma extravasation induced by electrical stimulation of the superior salivatory nucleus in cat nasal mucosa

The effects of electrical stimulation, applied to the superior salivatory nucleus (SSN) or the cervical sympathetic nerve, on vascular permeability in nasal mucosa were studied in 16 cats. Plasma extravasation was quantified by using Evans blue. Vascular permeability in the cat nasal mucosa was increased by the electrical stimulation of SSN. Plasma extravasation induced by SSN stimulation was reduced by administration of nitric oxide synthase (NOS) antagonist, N(omega)-nitro-L-arginine methyl ester (L-NAME). Administration of atropine did not affect increased vascular permeability by SSN stimulation. We conclude that neurogenic plasma extravasation in cat nasal mucosa evoked by the parasympathetic nerve is not mediated by cholinergic fibers but rather by nitric oxide.

1616 Influences of vagal afferent inputs on respiratory rhythm during induced vocalization

To investigate the genesis of respiratory neural rhythm in the mammalian spinal cord, we experimentally induced the spinal respiratory rhythm in rib-attached spinal cord preparations (decerebrated at the upper cervical level) isolated from neonatal rats (0 3 days). Phrenic burst discharges were recorded unilaterally from a phrenic nerve by a suction electrode. Serotonin (54-R, 50 w) was bath-applied for 5 min into the recording chamber with a perfusate (modified Krebs’, 25 27 ‘C). From 1 to 2 minutes after the 5-HT application, tetanic contraction of the rib cage occurred and then followed by rhythmic contraction-relaxations of flexors of neck and the rib cage with a period of 10 30 s. Concomitantly with the muscle contraction-relaxation cycles, the phrenic bursts were recorded with a duration of 5 10 s. These bursts synchronized with the contraction rhythm locked to the relaxation phase. These results clearly demonstrate that the spinal cord has an ability for generating respiratory rhythm.